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Home / Drugs / Starting with L / Lidocaine

A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of procaine but its duration of action is shorter than that of bupivacaine or prilocaine. [PubChem]
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CategoriesAntiarrhythmic Agents
Anesthetics, Local
Anti-Arrhythmia Agents
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For production of local or regional anesthesia by infiltration techniques such as percutaneous injection and intravenous regional anesthesia by peripheral nerve block techniques such as brachial plexus and intercostal and by central neural techniques such as lumbar and caudal epidural blocks.


Lidocaine is an anesthetic agent indicated for production of local or regional anesthesia and in the treatment of ventricular tachycardia occurring during cardiac manipulation, such as surgery or catheterization, or which may occur during acute myocardial infarction, digitalis toxicity, or other cardiac diseases. The mode of action of the antiarrhythmic effect of Lidocaine appears to be similar to that of procaine, procainamide and quinidine. Ventricular excitability is depressed and the stimulation threshold of the ventricle is increased during diastole. The sinoatrial node is, however, unaffected. In contrast to the latter 3 drugs, Lidocaine in therapeutic doses does not produce a significant decrease in arterial pressure or in cardiac contractile force. In larger doses, lidocaine may produce circulatory depression, but the magnitude of the change is less than that found with comparable doses of procainamide.

mechanism of action

Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses thereby effecting local anesthetic action. Lidocaine alters signal conduction in neurons by blocking the fast voltage gated sodium (Na+) channels in the neuronal cell membrane that are responsible for signal propagation. With sufficient blockage the membrane of the postsynaptic neuron will not depolarize and will thus fail to transmit an action potential. This creates the anaesthetic effect by not merely preventing pain signals from propagating to the brain but by aborting their birth in the first place.


The oral LD 50 of lidocaine HCl in non-fasted female rats is 459 (346-773) mg/kg (as the salt) and 214 (159-324) mg/kg (as the salt) in fasted female rats. Symptoms of overdose include convulsions, hypoxia, acidosis, bradycardia, arrhythmias and cardiac arrest.


Primarily hepatic.


Information derived from diverse formulations, concentrations and usages reveals that lidocaine is completely absorbed following parenteral administration, its rate of absorption depending, for example, upon various factors such as the site of administration and the presence or absence of a vasoconstrictor agent.

half life

109 minutes

route of elimination

Lidocaine and its metabolites are excreted by the kidneys.

drug interactions

Acebutolol: The beta-blocker, acebutolol, may increase the effect and toxicity of lidocaine.

Atazanavir: Increased risk of cardiotoxicity and arrhythmias

Atenolol: The beta-blocker, atenolol, may increase the effect and toxicity of lidocaine.

Bisoprolol: The beta-blocker, bisoprolol, may increase the effect and toxicity of lidocaine.

Carvedilol: The beta-blocker, carvedilol, may increase the effect and toxicity of lidocaine.

Cimetidine: Increases the effect and toxicity of lidocaine

Darunavir: Possible increase in lidocaine levels

Esmolol: The beta-blocker, esmolol, may increase the effect and toxicity of lidocaine.

Labetalol: The beta-blocker, labetalol, may increase the effect and toxicity of lidocaine.

Metoprolol: The beta-blocker, metoprolol, may increase the effect and toxicity of lidocaine

Nadolol: The beta-blocker, nadolol, may decrease symptoms of hypoglycemia.

Oxprenolol: The beta-blocker increases the effect and toxicity of lidocaine

Pindolol: The beta-blocker increases the effect and toxicity of lidocaine

Propranolol: The beta-blocker, propranolol, may increase the effect and toxicity of lidocaine.

Quinupristin: This combination presents an increased risk of toxicity

Tacrine: The metabolism of Tacrine, a CYP1A2 substrate, may be reduced by strong CYP1A2 inhibitors such as Lidocaine. Consider modifying therapy to avoid Tacrine toxicity. Monitor the efficacy and toxicity of Tacrine if Lidocaine is initiated, discontinued or if the dose is changed.

Tamoxifen: Lidocaine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Consider alternate therapy.

Tamsulosin: Lidocaine, a CYP3A4/2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4/2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Lidocaine is initiated, discontinued, or dose changed.

Telithromycin: Telithromycin may reduce clearance of Lidocaine. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Lidocaine if Telithromycin is initiated, discontinued or dose changed.

Terbinafine: Terbinafine may reduce the metabolism and clearance of Lidocaine. Consider alternate therapy or monitor for therapeutic/adverse effects of Lidocaine if Terbinafine is initiated, discontinued or dose changed.

Thiothixene: The strong CYP1A2 inhibitor, Lidocaine, may decrease the metabolism and clearance of Thiothixene, a CYP1A2 substrate. Consider alternate therapy or monitor for changes in Thiothixene therapeutic and adverse effects if Lidocaine is initiated, discontinued or dose changed.

Timolol: The beta-blocker, timolol, may increase the effect and toxicity of lidocaine.

Tizanidine: Lidocaine may decrease the metabolism and clearance of Tizanidine. Consider alternate therapy or use caution during co-administration.

Tolterodine: Lidocaine may decrease the metabolism and clearance of Tolterodine. Adjust Tolterodine dose and monitor for efficacy and toxicity.

Tramadol: Lidocaine may increase Tramadol toxicity by decreasing Tramadol metabolism and clearance. Lidocaine may decrease the effect of Tramadol by decreasing active metabolite production.

Trazodone: The CYP3A4 inhibitor, Lidocaine, may increase Trazodone efficacy/toxicity by decreasing Trazodone metabolism and clearance. Monitor for changes in Trazodone efficacy/toxicity if Lidocaine is initiated, discontinued or dose changed.

Voriconazole: Voriconazole, a strong CYP3A4 inhibitor, may increase the serum concentration of lidocaine by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of lidocaine if voriconazole is initiated, discontinued or dose changed.